WANG Xin-jin , CHANG Xiu-li , ZHOU Zhi-jun . Methylmercury Tunes Cell Cycle Regulated Gene Expressions in Human Embryonic Neural Stem Cells through miRNAs[J]. Journal of Environmental and Occupational Medicine, 2015, 32(5): 455-459. DOI: 10.13213/j.cnki.jeom.2015.14788
Citation: WANG Xin-jin , CHANG Xiu-li , ZHOU Zhi-jun . Methylmercury Tunes Cell Cycle Regulated Gene Expressions in Human Embryonic Neural Stem Cells through miRNAs[J]. Journal of Environmental and Occupational Medicine, 2015, 32(5): 455-459. DOI: 10.13213/j.cnki.jeom.2015.14788

Methylmercury Tunes Cell Cycle Regulated Gene Expressions in Human Embryonic Neural Stem Cells through miRNAs

  • Objective To investigate the impact on alteration of cell cycle regulated genes induced by low-level methylmercury via the expression of microRNAs of human embryonic neural stem cells.

    Methods After treatment with 0,10,and 50 nmol/L methylmercury for 24 h to human embryonic neural stem cells,cell viability was measured with methyl thiazolyl tetrazolium (MTT) assay.mRNA expressions of cell cycle regulated genes p16 and p21 were determined in human embryonic stem cells after the methylmercury exposure by reverse transcription polymerase chain reaction (RT-PCR).Expressions of miRNA (miR-24 and miR-106a) were determined using quantitative real time polymerase chain reaction (qRT-PCR) assay.

    Results Compared with the control group,the cell viability was significantly reduced by 53.5% in the 50 nmol/L methylmercury treatment group (P < 0.05).Compared with the control group,RT-PCR analysis revealed significant methylmercury-induced up-regulations of p16 and p21 mRNA expressions (P < 0.05),but no difference in p16 expression level was found between the 10 nmol/L and the 50 nmol/L treatment.The expressions of miR-24 and miR-106a were significantly lower with the increases in methylmercury concentrations (P < 0.05).

    Conclusion Methylmercury treatment at 50 nmol/L could restrain the self-renewal ability of neural stem cells and tune cell cycle regulators transcription through altering the expression of miRNAs.

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